1. Syncope A Diagnostic and Treatment Strategy
Toni M. Aprami, dr., Sp.PD, Sp.JP(K), FIHA, FAsCC
Department of Cardiology and Vascular Medicine
Division of Cardiovascular, Department of Internal Medicine
Padjadjaran University School of Medicine/Hasan Sadikin Hospital , Bandung

2. Transient Loss of Consciousness (TLOC)
Transient Loss of Consciousness, or TLOC, is just that.
It can be as simple as a benign ‘faint’ or a symptom of an underlying disease that may lead to sudden death. Or it may not be syncope at all.

3. Classification of Transient Loss of Consciousness (TLOC)
Real or Apparent TLOC
Syncope
Neurally-mediated reflex syndromes
Orthostatic hypotension
Cardiac arrhythmias
Structural cardiovascular disease
Disorders Mimicking Syncope
With loss of consciousness, i.e., seizure disorders, contussion
Without loss of consciousness, i.e., psychogenic “pseudo-syncope”
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

4. Syncope – A Symptom, Not a Diagnosis
Self-limited loss of consciousness and postural tone
Relatively rapid onset
Variable warning symptoms
Spontaneous, complete, and usually prompt recovery without medical or surgical intervention
Underlying mechanism is transient global cerebral hypoperfusion.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

5. III. Specific Conditions and Treatment
Overview
I. Etiology
II. Diagnosis
III. Specific Conditions and Treatment

6. Etiology

7. Unexplained Causes = Approximately 1/3
Causes of True Syncope
Neurally-
Mediated
Orthostatic
Cardiac
Arrhythmia
Structural
Cardio-
Pulmonary 1
VVS
CSS
• Situational
Cough
Post-
Micturition 2
Drug-Induced
• ANS Failure
Primary
Secondary 3
Brady
SAN Dysfunction
AV Block
• Tachy VT
SVT
Long QT Syndrome 4
Acute Myocardial Ischemia
Aortic Stenosis
HCM
Pulmonary Hypertension
Aortic Dissection
This slide provides a simple classification of the principal causes of syncope, listed from the most commonly observed (left) to the least common (right). This ranking may be helpful in thinking about the strategy for evaluating syncope in individual patients.
Within the boxes, the most common causes of syncope are indicated for each of the major diagnostic groups.
The terms ‘neurally-mediated syncope’, ‘neurally-mediated reflex syncope,’ and ‘neurocardiogenic syncope’ are generally used synonymously. For purposes of this presentation, ‘neurally-mediated syncope’ is used to define a broad category; ‘neurocardiogenic’ or ‘vasovagal syncope’ refer to a specific condition.
VVS—Vasovagal Syncope
CSS—Carotid Sinus Syndrome
ANS—Autonomic Nervous System
HCM—Hypertrophic Cardiomyopathy
DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
Unexplained Causes = Approximately 1/3
VVS : Vasovagal Syndrome ; CSS : Carotid Sinus Syndrome

8. Syncope Mimics Acute intoxication (e.g., alcohol) Seizures
Sleep disorders
Somatization disorder (psychogenic pseudo-syncope)
Trauma/contussion
Hypoglycemia
Hyperventilation
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

9. Impact of Syncope
40% will experience syncope at least once in a lifetime1
1-6% of hospital admissions2
1% of emergency room visits per year3,4
10% of falls by elderly are due to syncope5
Major morbidity reported in 6%1 eg, fractures, motor vehicle accidents
Minor injury in 29%1 eg, lacerations, bruises
1Kenny RA, Kapoor WN. Epidemiology and social costs. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura;2003:23-27.
2Kapoor W. Evaluation and outcome of patients with syncope. Medicine. 1990;69:
3Brignole M, Disertori M, Menozzi C, et al. Management of syncope referred urgently to general hospitals with and without syncope units. Europace. 2003;5:
4 Blanc J-J, L’ Her C, Touiza A, et al. Prospective evaluation and outcome of patients admitted for syncope over a 1 year period. Eur Heart J. 2002;23:
5Campbell A, Reinken J, Allan B, et al. Falls in old age: A study of frequency and related clinical factors. Age and Ageing. 1981;10:
1Kenny RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27.
2Kapoor W. Medicine. 1990;69:
3Brignole M, et al. Europace. 2003;5:
4 Blanc J-J, et al. Eur Heart J. 2002;23:
5Campbell A, et al. Age and Ageing. 1981;10:

10. Implications of Syncope for Driving a Vehicle
Those who drive and have recurrent syncope risk their lives and the lives of others
Places considerable burden on the physician
Essential to know local laws and physician responsibilities
Some states – Invasion of privacy to notify motor vehicle department*
Other states – Reporting is mandatory*
If the patient has sufficient warning of impending syncope – Driving may be permitted
Olshansky B, Grubb B. Driving and Syncope. In: Olshansky B and Grubb B, eds. Syncope: Mechanisms and Management. Armonk, NY: Futura Publishing Co; 1998:
*Medtronic, Inc. When may patients with implanted defibrillators drive? Follow-up Forum. Winter. 1995/96;1(3):8-10.
Olshansky B, Grubb B. In: Syncope: Mechanisms and Management. Futura. Armonk, NY
*Medtronic, Inc. Follow-up Forum. 1995/96;1(3):8-10.

11. Quality of life implications
Challenges of Syncope
Diagnosis
Complex
Quality of life implications
Work
Mobility (automobiles)
Psychological
Cost
Cost/year
Cost/diagnosis
Syncope impacts patient quality of life and health care costs in important ways.
Establishing a precise diagnosis is often challenging due to the unpredictability of events and the limited positive predictive value of most available tests. The ‘gold standard’ remains the recording of the cardiac rhythm (and if possible the arterial pressure) during a spontaneous faint.

12. Diagnosis

13. Diagnostic Objectives
Distinguish true syncope from syncope mimics
Determine presence of heart disease
Establish the cause of syncope with sufficient certainty to:
Assess prognosis confidently
Initiate effective preventive treatment

14. A Diagnostic Plan is Essential
Initial Examination
Detailed patient history
Physical exam
ECG
Supine and upright blood pressure
Monitoring
Holter
Event
Insertable Loop Recorder (ILR)
Cardiac Imaging
Special Investigations
Head-up tilt test
Hemodynamics
Electrophysiology study
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

15. Diagnostic Flow Diagram for TLOC
Initial Evaluation
Treatment
Syncope
Not Syncope
Certain Diagnosis
Unexplained Syncope
Cardiac Likely
Cardiac Tests
Neurally-Mediated or Orthostatic Likely
Tests for Neurally-Mediated Syncope
Frequent or Severe Episodes
Single/Rare Episodes
No Further Evaluation
Confirm with Specific Test or Specialist Consultation
Suspected Diagnosis + -
Re-Appraisal
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

16. Initial Exam: Detailed Patient History
Circumstances of recent event
Eyewitness account of event
Symptoms at onset of event
Sequelae
Medications
Circumstances of more remote events
Concomitant disease, especially cardiac
Pertinent family history
Cardiac disease
Sudden death
Metabolic disorders
Past medical history
Neurological history
Syncope
The history must include detailed summary of events leading up to and following syncope events. Additionally, it is important to ascertain whether there is any evidence of underlying structural heart disease. The direction of subsequent evaluation differs in patients with and without heart disease.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Raviele A, Alboni P, Sutton D, Kenny RA. Initial evaluation of the syncope patient. In: Benditt D, Blanc J-J, Brignole M, Sutton R, eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura. 2003:38-45.
Brignole M, et al. Europace, 2004;6:

17. Initial Exam: Thorough Physical
Vital signs
Heart rate
Orthostatic blood pressure change
Cardiovascular exam: Is heart disease present?
ECG: Long QT, pre-excitation, conduction system disease
Echo: LV function, valve status, HCM
Neurological exam
Carotid sinus massage
Perform under clinically appropriate conditions preferably during head-up tilt test
Monitor both ECG and BP
HCM—Hypertrophic Cardiomyopathy
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

18. Carotid Sinus Massage (CSM)
Method1
Massage, 5-10 seconds
Don’t occlude
Supine and upright posture (on tilt table)
Outcome
3 second asystole and/or mmHg fall in systolic BP with reproduction of symptoms = Carotid Sinus Syndrome
Absolute contraindications2
Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months
Complications
Primarily neurological
Less than 0.2%3
Usually transient
Carotid sinus massage (CSM) is an often overlooked, yet highly cost effective test, especially in older syncope patients. CSM must be applied with care, and the method described here1 has proven both safe and effective.
Note that an abnormal response to CSM (i.e., Carotid Sinus Hypersensitivity, CSH) is not diagnostic of Carotid Sinus Syndrome (CSS). Reproduction of symptoms is a crucial diagnostic element. To achieve symptom reproduction, it may be useful to conduct CSM with the patient in the upright posture. If the latter is to be done, the patient should be safely secured to a tilt table in order to prevent injury from a fall.
1Kenny RA, O’Shea D, Parry SW. The Newcastle protocols for head-up tilt table testing in the diagnosis of vasovagal syncope, carotid sinus hypersensitivity, and related disorders. Heart. 2000;83:
2Linzer M, Yang EH, Estes M, et al. Diagnosing Syncope: Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):
3Munro N, McIntosh S, Lawson J, et al. Incidence of complications after carotid sinus massage in older patients with syncope. J Am Geriatr Soc. 1994;42:
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
1Kenny RA. Heart. 2000;83:564. 2Linzer M. Ann Intern Med. 1997;126:989.
3Munro N, et al. J Am Geriatr Soc. 1994;42:

19. Other Diagnostic Tests
Ambulatory ECG
Holter monitoring
Event recorder
Intermittent vs. Loop
Insertable Loop Recorder (ILR)
Head-Up Tilt (HUT)
Includes drug provocation (NTG, isoproterenol)
Carotid Sinus Massage (CSM)
Adenosine Triphosphate Test (ATP)
Electrophysiology Study (EPS)
NTG = nitroglycerin
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

20. Neurological Tests: Rarely Diagnostic for Syncope
EEG, Head CT, Head MRI
May help diagnose seizure
Neurological studies (Head CT and MRI, EEG) are rarely useful in the diagnostic evaluation for syncope. Imaging may be justified if there is concern that syncope may have resulted in a head injury. Otherwise, without apparent abnormal neurological signs, such testing should be relegated to low priority.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace. 2004;6:

21. Head-Up Tilt Test (HUT)
Protocols vary
Useful as diagnostic adjunct in atypical syncope cases
Useful in teaching patients to recognize prodromal symptoms
Not useful in assessing treatment
60° - 80°
The rationale for undertaking tilt table testing in patients suspected of having vasovagal (VVS) syncope is summarized here. The test may provide useful diagnostic information and also an opportunity for patients to become more familiar with the condition and its possible warning signs.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace. 2004;6:

22. Insertable Loop Recorder (ILR)
The Reveal® Plus Insertable Loop Recorder system offers long-term, continuous, subcutaneous ECG monitoring and event-specific recording. The system includes an implanted loop recorder, a hand-held patient Activator, and a programmer with telemetry head that communicates noninvasively with the implanted device.
When a patient experiences an episode, the device stores an ECG using the Activator or through the use of a auto-activating feature.
The Reveal® Plus ILR can monitor continuously for up to 14 months. The probability of capturing an event is high—approximately 65-88%.1,2
The ECG captured during the episode may “reveal” the ECG during the patient’s episode or may allow the clinician to rule in or rule out arrhythmic causes.
The stored ECG data is retrieved, viewed, and printed or saved to a disk, using a Medtronic programmer. The Reveal ILR can then be re-started for continued monitoring.
1Krahn A, et al. Final results from a pilot study with an insertable loop recorder to determine the etiology of syncope in patients with negative noninvasive and invasive testing. Am J Cardiol. 1998;82:
2Krahn A, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial. Conventional diagnostic testing versus a prolonged monitoring strategy. Circulation. 2001;104:46-51.
Click once on black screen to play video.
Reveal® Plus ILR
Typical Location of the Reveal® Plus ILR

23. Insertable Loop Recorder (ILR)
The ILR is an implantable patient – and automatically – activated monitoring system that records subcutaneous ECG and is indicated for:
Patients with clinical syndromes or situations at increased risk of cardiac arrhythmias
Patients who experience transient symptoms that may suggest a cardiac arrhythmia

24. Specific Conditions and Treatment
The next section deals with some of the more important causes of syncope.

25. Specific Conditions Cardiac arrhythmia Structural cardio-pulmonary
Brady/Tachy
Long QT syndrome
Torsade de pointes
Brugada
Drug-induced
Structural cardio-pulmonary
Neurally-mediated
Vasovagal Syncope (VVS)
Carotid Sinus Syndrome (CSS)
Orthostatic

26. Cardiac Syncope Includes cardiac arrhythmias and SHD
Often life-threatening
May be warning of critical CV disease
Tachy and brady arrhythmias
Myocardial ischemia, aortic stenosis, pulmonary hypertension, aortic dissection
Assess culprit arrhythmia or structural abnormality aggressively
Initiate treatment promptly
Syncope occurring as a result of cardiac arrhythmias or in association with underlying structural heart disease requires careful and aggressive evaluation. Whereas syncope in patients with normal hearts is often relatively benign, syncope in the presence of cardiac disease is often indicative of a potentially life-threatening problem.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace. 2004;6:

27. Syncope Due to Structural Cardiovascular Disease: Principle Mechanisms
Acute MI/Ischemia
2° neural reflex bradycardia – Vasodilatation, arrhythmias, low output (rare)
Hypertrophic cardiomyopathy
Limited output during exertion (increased obstruction, greater demand), arrhythmias, neural reflex
Acute aortic dissection
Neural reflex mechanism, pericardial tamponade
Pulmonary embolus/ pulmonary hypertension
Neural reflex, inadequate flow with exertion
Valvular abnormalities
Aortic stenosis – Limited output, neural reflex dilation in periphery
Mitral stenosis, atrial myxoma – Obstruction to adequate flow
This slide lists important structural cardiovascular abnormalities to be considered during the diagnostic evaluation of syncope.
Obstruction of blood flow and arrhythmias are often the mechanisms for the syncope; all are high risk.
The list is not intended to be exhaustive of the possibilities, but provides some of the more commonly found conditions.
MI—myocardial infarction
HCM—hypertrophic cardiomyopathy
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace. 2004;6:

28. Syncope Due to Cardiac Arrhythmias
Bradyarrhythmias
Sinus arrest, exit block
High grade or acute complete AV block
Can be accompanied by vasodilatation (VVS, CSS)
Tachyarrhythmias
Atrial fibrillation/flutter with rapid ventricular rate (eg, pre-excitation syndrome)
Paroxysmal SVT or VT
Torsade de pointes
Both excessively slow as well as excessively rapid heart rates may result in sufficient drop in systemic pressure to cause syncope. In the case of tachycardias, the syncope tends to occur at the onset of the episode, before vascular constriction has an opportunity to occur. Syncope may also occur at termination of tachyarrhythmias, if a prolonged pause occurs prior to resumption of a stable rhythm.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace. 2004;6:

29. ILR Recordings
These are Reveal® ILR recordings from patients with syncopal symptoms. The left recording was obtained in an 83 year old woman and suggests bradycardic episodes as a cause of syncope. The right recording was obtained in a younger patient with idiopathic ventricular tachycardia.
Reveal ® ILR recordings; Medtronic data on file.
CASE: 83 year-old woman with syncope due to bradycardia: Pacemaker implanted.
CASE: 28 year-old man presents to ER multiple times after falls resulting in trauma. VT: Ablated and medicated.
Reveal ® ILR recordings; Medtronic data on file.

30. Long QT Syndromes Mechanism Prevalence
Abnormalities of sodium and/or potassium channels
Susceptibility to polymorphic VT (Torsade de pointes)
Prevalence
Drug-induced forms – Common
Genetic forms – Relatively rare, but increasingly being recognized
“Concealed” forms:
May be common
Provide basis for drug-induced torsade
Schwartz P and Priori S. Long QT syndrome: Genotype-Phenotype correlations. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia, PA: Saunders;2004:
Schwartz P, Priori S. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. Saunders;2004:

31. Syncope: Torsade de Pointes
Torsade de pointes ventricular tachycardia often presents as syncope, although life-threatening sustained tachyarrhythmias may also occur. The underlying factors are most often either acquired or congenital long QT syndrome.
In this case, the patient had been treated with quinidine for several weeks in an attempt to suppress episodes of atrial fibrillation.
From the files of DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
From the files of DG Benditt, MD. U of M Cardiac Arrhythmia Center

32. Long QT Syndromes: 12-Lead ECG
From the files of DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
From the files of DG Benditt, MD. U of M Cardiac Arrhythmia Center

33. Drug-Induced QT Prolongation (List is continuously being updated)
Antiarrhythmics
Class IA ...Quinidine, Procainamide, Disopyramide
Class III…Sotalol, Ibutilide, Dofetilide, Amiodarone, NAPA*
Antianginal Agents
Bepridil*
Psychoactive Agents
Phenothiazines, Amitriptyline, Imipramine, Ziprasidone
Antibiotics
Erythromycin, Pentamidine, Fluconazole, Ciprofloxacin and its relatives
Nonsedating antihistamines
Terfenadine*, Astemizole
Others
Cisapride*, Droperidol, Haloperidol
Numerous drugs have been associated with QT interval prolongation leading to susceptibility to torsade de pointes ventricular tachycardia. Some of these agents have been removed from the market in the USA, as noted with an asterisk.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
*Removed from U.S. Market
Brignole M, et al. Europace, 2004;6:

34. Treatment of Long QT Suspicion and recognition are critical
Emergency treatment
Intravenous magnesium
Pacing to overcome bradycardia or pauses
Isoproterenol to increase heart rate and shorten repolarization
ICD if prior SCA or strong family history
If drug induced:
Reverse bradycardia
Withdraw drug
Avoid ALL long-QT provoking agents
If genetic:
For more information visit
Schwartz P and Priori S. Long QT syndrome: Genotype-Phenotype correlations. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia, PA: Saunders;2004:
Schwartz P, Priori S. In: Zipes D and Jalife J, eds. Cardiac Electrophysiology. Saunders;2004:

35. Treatment of Syncope Due to Bradyarrhythmia
Class I indication for pacing using dual chamber system wherever possible
Ventricular pacing in atrial fibrillation with slow ventricular response nV
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The treatment of syncope associated with bradyarrhythmias resulting from intrinsic conduction system disease is usually cardiac pacing. On occasion, removal of an offending drug may be sufficient. The problem of neurally-mediated reflex bradyarrhythmias is dealt with separately.
ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices: Summary Article. Circulation. 2002;106:
ACC/AHA/NASPE 2002 Guideline Update. Circ. 2002;106:

36. Treatment of Syncope Due to Tachyarrhythmia
Atrial tachyarrhythmias
AVRT due to accessory pathway – Ablate pathway
AVNRT – Ablate AV nodal slow pathway
Atrial fib – Pacing, linear/focal ablation for paroxysmal AF
Atrial flutter – Ablate the IVC-TV isthmus of the re-entrant circuit for ‘typical’ flutter
Ventricular tachyarrhythmias
Ventricular tachycardia – ICD or ablation where appropriate
Torsade de pointes – Withdraw offending drug or implant ICD (long QT/Brugada/short QT)
Drug therapy may be an alternative in many cases
This slide provides an overview of the multiple tachyarrhythmias that may cause syncope. An EP study has proven more valuable in assessing tachyarrhythmia causes of syncope than those due to bradycardia.
IVC-TV =Inferior Vena Cava-Tricuspid Valve
AVRT =Atrioventricular Reentry Tachycardia
AVNRT =Atrioventricular Nodal Reentry Tachycardia
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace. 2004;6:

37. Neurally-Mediated Reflex Syncope
Vasovagal Syncope (VVS)
Carotid Sinus Syndrome (CSS)
Situational syncope
Post-micturition
Cough
Swallow
Defecation
Blood drawing, etc.
The neurally-mediated reflex causes of syncope are a group of related conditions in terms of symptomatic hypotension being caused by a variable combination of bradycardia and vasodilatation.
Vasovagal syncope and carotid sinus syndrome are the most frequent conditions in this group. The others occur occasionally and are usually recognized only if a detailed medical history is obtained.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

38. Autonomic Nervous System
Pathophysiology
Autonomic Nervous System
The physiology of syncope is depicted graphically in this slide. The afferent trigger signals (eg, pain, emotional upset, dehydration) are not depicted. In the efferent loop of the neural reflex:
Parasympathetic signals from the cerebral cortex reduce heart rate and slow (or block) AV conduction.
Decreased sympathetic activity results in vasodilatation.
Bradycardia and/or hypotension occur.
Carotid baroreceptors and other mechanoreceptors provide paradoxical feedback to the central nervous system, aggravating bradycardia and vasodilatation.
The result may be a downward spiral in heart rate and blood pressure leading to syncope.
Benditt DG, Lurie KG, Adler SW, et al. Pathophysiology of vasovagal syncope. In: Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, Benditt D, Sutton R. Bakken Research Center Series, v. 10. Armonk, NY: Futura, 1996.
Benditt D, et al. Neurally mediated syncope: Pathophysiology, investigations and treatment. Blanc JJ, et al. eds. Futura

39. VVS Clinical Pathophysiology
Neurally-mediated physiologic reflex mechanism with two components:
1. Cardioinhibitory (↓ HR)
2. Vasodepressor (↓ BP) despite heart beats, no significant BP generated
Both components are usually present 1
Vasovagal syncope, as in other forms of neurally-mediated reflex syncope, is due to systemic hypotension resulting in a transient period of inadequate cerebral blood flow.
Hypotension is the result of two pathophysiologic components:
Marked bradycardia or inappropriately slow heart rate for the blood pressure (i.e., cardioinhibitory feature)
Vasodilatation
The relative contribution of these two components varies among patients.
Wieling W, Gert van Dijk J, van Lieshout J, Benditt D. Pathophysiology and clinical presentation. In: Benditt D, Blanc J-J, et al. eds. The Evaluation and Treatment of Syncope. Elmsford, NY: Futura. 2003;11-22. 2
Wieling W, et al. In: Benditt D, et al. The Evaluation and Treatment of Syncope. Futura. 2003;11-22.

40. VVS Incidence Most common form of syncope
8% to 37% (mean 18%) of syncope cases
Depends on population sampled
Young without SHD, ↑ incidence
Older with SHD, ↓ incidence
The incidence of vasovagal syncope is poorly known.
The published data that exists mostly dates from before the advent of tilt table testing.
Linzer surveyed the literature and found published prevalences varying from 8% to 37% (mean 18%) of cases of syncope.
Standards for diagnosis and reporting are still emerging.
Linzer MD, Yang EH, Estes M, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):
Linzer M, et al. Ann Intern Med. 1997;126:989.

41. VVS vs. CSS In general: VVS patients younger than CSS patients
Ages range from adolescence to older adults (median 43 years)
It is generally recognized that:
Vasovagal syncope patients are usually younger than Carotid Sinus Syndrome patients (age range is from adolescent to older adults, median 43 years)
Vasovagal syncope is more common in females.
Linzer MD, Yang EH, Estes M, et al. Diagnosing syncope. Part 1: Value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):
Linzer M, et al. Ann Intern Med. 1997;126:989.

42. VVS Spontaneous
16 year-old male, healthy, athletic, monitored for fainting.
16.3
sec
Continuous Tracing
1 sec
Example of marked bradycardia recorded during a spontaneous vasovagal syncope. The asystolic periods may be impressive in their duration but do not in themselves constitute an indication for cardiac pacing.
From the files of DG Benditt, MD. University of Minnesota Cardiac Arrhythmia Center
From the files of DG Benditt, MD. U of M Cardiac Arrhythmia Center

43. VVS Diagnosis History and physical exam, ECG and BP
Head-Up Tilt (HUT) – Protocol:
Fast > 2 hours
ECG and continuous blood pressure, supine, and upright
Tilt to 70°, 20 minutes
Isoproterenol/Nitroglycerin if necessary
End point – Loss of consciousness
60° - 80°
Vasovagal syncope is most effectively diagnosed if the detailed medical history is ‘classic’. However, this is not often the case, and supporting evidence is needed. Such supportive evidence may include:
Patient history, physical examination, including ECG and blood pressure
Patient experiences syncope during tilt table testing. Test completion without syncope is a negative result.
The following is one tilt table protocol:
At least a 2 hour fast
Measure ECG, at least 3 leads, and continuous supine and upright blood pressure at time of symptoms.
Patient remains supine on the table for minutes.
Tilt to 70 degrees for 20 minutes.
Lower to horizontal and administer isoproterenol at 1-5 μg/min until heart rate increases 25%.
Re-tilt for 10 minutes
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Benditt D, Ferfuson D, Grubb B, et al. Tilt table testing for assessing syncope. ACC expert consensus document. J Am Coll Cardiol. 1996;28:
Benditt D, et al. JACC. 1996;28:
Brignole M, et al. Europace, 2004;6:

44. VVS General Treatment Measures
Optimal treatment strategies for VVS are a source of debate
Treatment goals
Acute intervention
Physical maneuvers, eg, crossing legs or tugging arms
Lowering head
Lying down
Long-term prevention
Tilt training
Education
Diet, fluids, salt
Support hose
Drug therapy
Pacing
Optimal management strategies for VVS are a source of debate. Long-term prevention measures include:
Patient education, reassurance, and instruction.
Control of fluids, salt, and diet may help reduce incidence.
Support hose may limit blood pooling in the legs and feet.
Drug therapy should be used as a second line option. Midodrine and beta-adrenergic blockers are the agents most thoroughly studied to date
Pacing may benefit some patients. Subsequent slides will examine the utility of pacing in very symptomatic VVS patients.
When the patient has a relatively long prodrome, evasive action may prevent injury if not syncope. This might include physical maneuvers such as crossing the legs, lowering the head, or lying down.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

45. VVS Tilt Training Protocol
Objectives
Enhance orthostatic tolerance
Diminish excessive autonomic reflex activity
Reduce syncope susceptibility/recurrences
Technique
Prescribed periods of upright posture against a wall
Start with 3-5 min BID
Increase by 5 min each week until a duration of 30 min is achieved
Reybrouck T, Heidbuchel H, Van de Werf F, Ector H, et al. Tilt training: A treatment for malignant and recurrent neurocardiogenic syncope. PACE. 2000;23(4 Pt. 1):
Reybrouck T, et al. PACE. 2000;23(4 Pt. 1):

46. CSS Etiology Carotid Sinus
Sensory nerve endings in the carotid sinus walls respond to deformation
“Deafferentation” of neck muscles may contribute
Increased afferent signals to brain stem
Reflex increase in efferent vagal activity and diminution of sympathetic tone results in bradycardia and vasodilatation
Carotid Sinus
The etiology of CSS rests in part from afferent signals arising in the carotid baroreceptors, and inappropriate concomitant signals from nearby neck muscles.
Sensory nerve endings in the carotid sinus walls respond to deformation.
An increase in afferent traffic results in cardioinhibition and vasodilatation.
Deafferentation of nearby neck muscles may contribute. The CNS is not informed of neck movement and consequently the carotid baroreceptor afferents are interpreted as indicating a rise in central arterial pressure.
Blanc JJ, L’Heveder J, Mansourati J, et al. Pathophysiology of carotid sinus syndrome. In: Neurally mediated syncope: Pathophysiology, investigation and treatment. Blanc JJ, Benditt D, Sutton R. eds. Armonk, NY: Futura;1996:25-29.
Kenny RA, McIntosh SJ. Carotid sinus syndrome. In: Syncope in the Older Patient. Kenny RA ed. London: Chapman & Hall Medical; 1996:

47. Orthostatic Hypotension
Etiology
Drug-induced (very common)
Diuretics
Vasodilators
Primary autonomic failure
Multiple system atrophy
Parkinson’s Disease
Postural Orthostatic Tachycardia Syndrome (POTS)
Secondary autonomic failure
Diabetes
Alcohol
Amyloid
Orthostatic hypotension is an important cause of syncope. The medical history is usually sufficient to establish the diagnosis. However, defining the specific cause requires careful consideration of a number of important conditions.
The most important conditions predisposing to orthostatic syncope are listed here.
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

48. Treatment Strategies for Orthostatic Intolerance
Patient education, injury avoidance
Hydration
Fluids, salt, diet
Minimize caffeine/alcohol
Sleeping with head of bed elevated
Tilt training, leg crossing, arm pull
Support hose
Drug therapies
Fludrocortisone, midodrine, erythropoietin
Tachy-Pacing (probably not useful)
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6:

49. Syncope: Diagnostic Testing in Hospital Strongly Recommended
Suspected/known ‘significant’ heart disease
ECG abnormalities suggesting potential life-threatening arrhythmic cause
Syncope during exercise
Severe injury or accident
Family history of premature sudden death
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace. 2004;6:

50. Conclusion Syncope is a common symptom with many causes
Deserves thorough investigation and appropriate treatment
A disciplined approach is essential
ESC guidelines offer current best practices
Brignole M, Alboni P, Benditt D, et al. Guidelines on management (diagnosis and treatment) of syncope—Update Europace. 2004;6:
Brignole M, et al. Europace, 2004;6: